Sanjoy Banerjee MD

Classification of Headaches

International Headache Society (IHS)

updated 2004

1. Primary- no causal pathology

2. Secondary- causal pathology

PRIMARY HEADACHES

Migraines- with aura

Migraine without aura

Tension Type Headache

Cluster headache and other trigeminal

autonomic cephalgias

Others- new persistent daily headache

SECONDARY HEADACHES Head/neck trauma

Cranial/cervical vascular Dz

Non vascular intracranial Dz

Substance abuse/ withdrawl

Infection

Homeostasis

Anatomic disorders of head/neck

Psychiatric Dz

Evaluation

Important to distinguish common

symptoms from life threatening ones.

Headache evaluation for 30 min consists

of 28 min headache history and 2 min

examination

Mechanisms of Headaches

Traction on intracranial structures- PDPH

Dilation of cranial arteries

Intracranial– cluster headaches, anoxia,CO2,pheocheochromocytoma

Extracranial- migraine or cluster

Inflamation- meningitis, temporal arteritis

Primary

Migraines,

Tension

type, cluster

headaches

90

10

Headaches

Primary

Secondary Secondary

Tumor, Meningitis,

Arteritis

Headache

Warning signs

present??•Primary

headache Secondary

headache

Investigations

YESNO

DIAGNOSTIC

EVALUATION

Signs of Secondary Headaches

1. sudden onset first/worse

2. sub acute with increasing frequency/severity

3. Headache with systemic illness-fever/rash/neck stiffness

4. Focal neurological signs- headache always on the same side

5. Chronic daily headache

6. papilledema, cognitive impairment, personality change, seizures

Sudden onset headache

Subarachnoid hemorrhage, bleed in to

mass lesion, AVM, mass lesion

Investigation- Neuroimaging, LP after

neuroimaging, not before….

Worsening Headache

Mass lesion, subdural

hematoma, medication overuse

Investigations- neuroimaging, careful

history of drug use.

Drug screen and levels

Headache with systemic illness

Meningitis, encephalitis, Lyme Dz, collagen

vascular Dz, opportunistic infections in

immunocompromised (chemo, HIV,DM,CA)

Investigations- neuroimaging, collagen

vascular evaluation, LP, Immune

w/u, infection w/u.

Focal Neurological Signs

Mass lesions, AVM, Collagen Vascular

DZ

Investigation- neuroimaging, collagen

vascular evaluation

Papilledema

Mass lesions, pseudo tumor cerebri, encephalitis, meningitis

Investigations- neuroimaging, LP after neuroimaging unless meningitis is strongly suspected and imaging not available

Primary Headaches Diagnosis of primary headache( no intracranial pathology)

has been defined by the IHS criteria in 1988 and modified in 2004.

Migraines with and without aura

Tension type headaches

Trigeminal autonomic cephalgias- cluster, paroxysmal hemicrania, SUNCT (short lasting, unilateral, neuralgiform headache with conjunctival injection and tearing)

Others-stabbing, cough, exertional, sexual, hypnic, thunderclap, hemicrania continua, new daily persistent headache

Migraine without Aura Features- At least 5 attacks

Lasts 4-72 hrs and occurs<15days/month

At least 2 of-

Unilateral location

pulsating nature

Moderate to severe pain

Aggravation/avoidance of routine physical activity

At least 1 of-

Nausea and or vomiting

Photophobia or phonophobia

Migraine with Aura Have to satisfy the previous criteria

PLUS

At least 2 migraine attacks and fully reversible sensory, visual, speech symptoms

At least 2 of

Visual or sensory phenomena

At least one symptom develops >5 min

Lasts < 60 min

Headache develops during or within 60min of aura

No other attributable disorder

Genetic Mechanisms

Migraine has a genetic mechanism but hereditary patters are unknown

Half the families with familial hemiplegic migraines show genetic linkage to chromosome 19p13. This affects P/Q type calcium channels.

Mechanism of Migraines

Vascular

Neurogenic

Pet Scan- activation of medial brainstem

structures during attack

Spreading depression during attack

Cont….. Neurovascular disorder causing dilation of pain

sensitive cranial blood vessels

Activation of trigeminal nerve fibers that innervate these vessels releasing algesic substances. Spreading of pain along all divisions of trigeminal nerve causing ocular and facial pain. Spreading to dorsal horn of C2,3,4 causing neck pain.

Activation of the cranial parasympathetic outflow

Trigeminal control of blood vessels

Mechanisms for 5HT 1D

CGRP

NK

SP

5-HT1F5-HT1D

5-HT1B

Blood vessel

Trigeminal

nerve

CGRP calcitonin gene

related peptide

NK neurokinin A

SP substance P

triptan

contriction

PET scan

showing

activation of

brainstem

during migraine

attack

Spreading Depression DURING AURA THERE IS

HYPOPERFUSION

of cerebral blood flow in gray matter of the posterior part of the hemisphere on contra lateral side of affected visual field or paresthesia

Reduced CBF moves slowly across cortex anteriorally. This reduces EEG activity.

This is called cortical spreading depression

Cerebral blood flow during Migraine

Cerebral Blood Flow

TIME

C

B

F Aura

PreHeadache

Post

Prodrome

premonitory symptoms

No premonitory symptoms

6040

-elated

Irritable

depressed

hungry

thirsty

Drowsy

25%

Post Headache

Phase

0% 20% 40% 60% 80%

Mood change

Muscle Weakness

Physical tiredness

Loss of apetite

Comorbidities with Migraine

Stroke

Epilepsy

SLE

Reynaud's

M.S

Hypertension

PFO/ MVP

Bipolar

Depression

Anxiety

Panic disorder

Simple and social

phobia

Psychiatric Comorbidity

Depression 25-80%

Resolves with effective headache Rx

Generalized Anxiety Disorder- 70%

Minnesota Multi phase personality test

abnormal in 60% -predicts intractability

Treatment of Migraine CONSERVATIVE

Removal of triggers-e.g.; tyramine, sleep deprivation, hypoglycemia, OCP, PMH Rx

Behavior mods-

Relaxation, biofeedback, stress management, CBT

MEDICAL Step care-

1. simple analgesics, NSAIDS

then-

2. Combination Rx –butalbitol/caffeine

then-

3. Specific migraine therapies- triptan

Treat to severity of symptoms

MIDAS disability

Scored questions

Results graded

Grade 1 score 0-5

Grade 2 score 6-10

Grade 3 score 11-20

Grade 4 score 21+

Minimal disability

Mild disability

Moderate disability

Severe disability

Pharmacological Agents

Analgesics- OTC, caffeine, nsaids for

mild attacks and low Midas scores

Abortive Rx- for severe attacks that

need to be prevented from occurring-

E.g.- Ergots, triptan. High Midas scores.

FDA Warning

Using Triptan with SSRI or SSNRI can cause Serotonin Syndrome.

It is accepted that Libby Zion law also known as the limiting of residency work hours by ACGME resulted from serotonin toxicity and death in Ms Zion due to overworked residents giving Demerol to a patient on phenelzine.(MAOI)

Prophylaxis of Migraines

Beta blockers

Ca channel blockers

Anticonvulsants

Propranolol

Verapamil

Topamax, valporate

Tension Type Headache

Features- At least 10 episodes occurring less than 1 day/month. No N/V, no more than 1 of photophobia or phonophobia.

2 of the following Bilateral location

Pressing/tightening non pulsatile

Mild/moderate intensity

Not aggravated by physical activity

Pathogenesis

Similar to migraine pathology

Precranial muscles are harder and more

tender in TTH patients

Nitric oxide synthetase inhibitor reduces

headache pain and central sensitization-

supporting NO mediated vasodilatation

Signs/Symptoms

Dull, achy, bilateral, non pulsatile

Sensation of pressing/tightening

No aggravation by physical activity

No N/V 1 of photo or phonophobia

No prodrome /aura

Severe pain is uncommon

Musculoskeletal component

Treatment

Prophylaxis-

greater than 2

headaches/week

Amitriptyline

Tizanidine

Triptan

Valporate, neurontin,

Topamax- speculative

Acute attack-

ASA,Tylenol,NSAID

Combo with caffeine

Isomethepthene

Butalbital

Cluster Headache Features-

Severe unilateral peri orbital, or temporal pain.

Lasts 15min-180min

Lacrimation, nasal congestion, rhinorrhea,

Facial swelling, miosis,

Ptosis, eyelid edema,

Conjunctival injection,

restlessness

IHS diagnostic criteria

Episodic-- occurs in periods of 7 days to 1 yr with at least 1 month remission

Chronic– lasts >1yr without remission

Pathology

Trigeminoautonomic distribution of

pain, autonomic features and periodicity

Neuropeptide release- VIP, CGRP

Neuroendocrine change- low testosterone

during attacks, low TSH

PET Scan- lights up in posterior

hypothalamic grey at base of 3rd ventricle

Cluster Headache Distribution

Relatively uncommon

Men>women

Ages 20-30’s

Genetic predisposition

Seasonal – spring

Most marked after 1st REM sleep

Treatment of Attack

100% O2 at 10L/min--- 60% effective

Sumatriptan SQ,IN,PO – 75% effective

Ergotamine 1mg IV (not with triptan)

IN lidocaine 6%-- 33% effective

Prophylaxis

Verapamil

Steroids

Methysergide

Ergotamine

Lithium

Valporate

?? Neurontin, Topamax, melatonin

Surgical Treatment

Occipital nerve block, sphenopalatine block

Percutaneous RF rhizotomy of retrogasserian ganglion

Gamma knife to ablate trigeminal nerve root

Percutaneous glycerol rhizolysis retrogasserian ganglion

Electro modulation of posterior hypothalamus

Chronic Daily Headaches

Chronic daily migraine, tension type, cluster.

Chronic paroxysmal hemicrania, hemicrania continua

New daily persistent headaches

Post traumatic headaches

Post craniotomy headaches

Medication overuse/ rebound headache

Chronic Daily Headache

0%

10%

20%

30%

40%

50%

60%

70%

80%

Headache Type

CM

CTTH

Others

Medication overuse/rebound

Migraine 65%, TTH 27%, others 8%

80% of patients with CDH have this

Female 3x greater than males

Usually occurs when

analgesic use >5days/wk

triptan use >3days/wk

opiod/ergot use >2days/wk

Treatment for CDH NO FDA APPROVED TREATMENT

TCA,SSRI,

B blockers, Verapamil,

Topamax, Neurontin,

NSAIS, muscle relaxants

Occipital nerve block

Botox A

Alpha 2 agonist- Tizanidine